Intracerebral Hemorrhage Caused by Cerebral Hyperperfusion after Superficial Temporal Artery to Middle Cerebral Artery Bypass for Atherosclerotic Occlusive Cerebrovascular Disease

Abstract

Few papers have reported detailed accounts of intracerebral hemorrhage caused by cerebral hyperperfusion after superficial temporal artery to middle cerebral artery bypass (STA-MCA) bypass for atherosclerotic occlusive cerebrovascular disease. We report a case of vasogenic edema and subsequent intracerebral hemorrhage caused by the cerebral hyperperfusion syndrome (CHS) after STA-MCA bypass for atherosclerotic occlusive cerebrovascular disease disease without intense postoperative blood pressure control. A 63-year-old man with repeating left hemiparesis underwent magnetic resonance angiography (MRA), which revealed right internal carotid artery (ICA) occlusion. We performed a double bypass superficial temporal artery (STA)-middle cerebral artery (MCA) bypass surgery for the M2 and M3 branches. While the patient's postoperative course was relatively uneventful, he suffered generalized convulsions, and computed tomography revealed a low area in the right frontal lobe on Day 4 after surgery. We considered this lesion to be pure vasogenic edema caused by cerebral hyperperfusion after revascularization. Intravenous drip infusion of a free radical scavenger (edaravone) and efforts to reduce systolic blood pressure to <120 mmHg were continued. The patient experienced severe left hemiparesis and disturbance of consciousness on Day 8 after surgery, due to intracerebral hemorrhage in the right frontal lobe at the site of the earlier vasogenic edema. Brain edema associated with cerebral hyperperfusion after STA-MCA bypass for atherosclerotic occlusive cerebrovascular disease should be recognized as a risk factor for intracerebral hemorrhage. The development of brain edema associated with CHS after STA-MCA bypass for atherosclerotic occlusive cerebrovascular disease requires not only intensive control of blood pressure, but also consideration of sedation therapy with propofol.

Keywords: atherosclerotic; cerebral hyperperfusion; extracranial–intracranial bypass; intracerebral hemorrhage.

Fig. 1

(A) Pre-operative magnetic resonance angiography (MRA) revealed right internal carotid artery (ICA) occlusion. (B) Post-operative MRA revealed good bypass patency.

Fig. 2

Single-photon emission computed tomography (SPECT) scan revealed a perfusion defect in the right frontal (hypoperfusion) and decreased cerebrovascular reactivity in the right hemisphere on the pre-operative with acetazolamide challenge test.

Fig. 3

(A) Pre-operative perfusion CT revealed at resting state revealed a perfusion defect (hypoperfusion) in the right frontal area of the right hemisphere. (B) Perfusion CT revealed hyperperfusion on Day 5 after surgery.

Fig. 4

(A) CT revealed no abnormalities on Day 1 after surgery. (B) CT revealed a low area in a right frontal on Day 4 after surgery. (C) CT revealed the right frontal intracerebral hemorrhage at the corresponding lesion to the prior vasogenic edema on Day 8 after surgery.

Fig. 5

(A) Magnetic resonance imaging (MRI) revealed the high intensity on T₂-weight on the day after Day 5 after surgery. (B) Magnetic resonance imaging (MRI) revealed slightly high on diffusion on the day after Day 5 after surgery.